The amount of fibrinogen-positive platelets predicts the occurrence of in-stent restenosis.

AIMS: To determine the value of fibrinogen-positive platelet-analysis in predicting restenosis after stent implantation in acute myocardial infarction patients. METHODS AND RESULTS: Our patient population comprised 50 patients who underwent intravascular ultrasound (IVUS) guided stent implantation for acute myocardial infarction. In all cases, IVUS confirmed a deep vessel wall injury due to a ruptured plaque within the culprit lesion. Flow cytometry quantified the amount of platelets with surface-bound fibrinogen and thrombospondin before and immediately after the intervention. After 5 months, IVUS was repeated to assess the long-term results. In-stent restenosis - defined as a percent diameter stenosis of >50% - was detected in 11 of 45 patients who attended follow-up angiography. The amount of fibrinogen-positive platelets was significantly higher among patients who subsequently developed in-stent restenosis (50.5+/-6.8% fibrinogen-positive platelets immediately after intervention) than among those who did not (39.7+/-12.3% fibrinogen-positive platelets, p<0.005). Receiver operating characteristic curve revealed a 40% cut-off for fibrinogen-positive platelets immediately after the intervention to predict restenosis (p<0.05, sensitivity: 90.9%, specificity: 47.1%). CONCLUSION: The amount of fibrinogen-positive platelets immediately after stent implantation predicts the occurrence of in-stent restenosis, as confirmed by IVUS in acute myocardial infarction patients.

Autoimmunological features in inflammatory cardiomyopathy.

During recent years, increasing evidence has been obtained that cellular as well as humoral autoimmunity is involved in the pathogenesis of dilated cardiomyopathy (DCM). The immune system is generally activated by viral infections with the objective of virus elimination from the myocardium. However, a relevant number of patients demonstrate viral persistence and/or chronic inflammation in the myocardium. This chronic myocardial inflammation, defined by chronic inflammation, is termed "inflammatory cardiomyopathy" according to the WHO classification of cardiomyopathies. Chronic inflammation is frequently followed by the development of autoimmunity. A breakdown in the control mechanisms protecting against autoimmune reactions by both presentation of normally not accessible self-antigens and bystander- activation, induced by the pathogen, leads to the formation of autoreactive antibodies and T cells. The auto-reactive antibodies interact directly with heart tissue resulting in altered signal transduction or complement activation, whereas the T cell-mediated mechanisms include direct attack by cytotoxic T cells or indirect effects of cytotoxic cytokines released by stimulated T cells or macrophages.